Alcohol and Substance misuse Flashcards

1
Q

What is the difference between harmful use and dependence?

A

Harmful use- patient can go days- weeks without alcohol but then binges to such an extent that it results in physical/ social harm.
Dependence- patient is preoccupied by alcohol, it affects their ADLs, they drink alone and have a narrow repetoire, drink to wake up, experience withdrawal symptoms if stop which include psychomotor agitation, loss of concentration + memory, tolerance and diff controlling intake- if start drinking cannot stop.

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2
Q

What is harmful substance use?

A

Harmful use describes engaging in bingeing behaviour and the continuation of substance use despite evidence of damage to the user’s physical or mental health or to their social, occupational or familial well-being. The damage may be denied or minimised by the individual concerned.

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3
Q

What is dependence?

A

Core features :

  1. PRIMACY: The drug and need to obtain it becomes the most important things in the person’s life taking priority over all other responsibilities, activities and interests. Relationships, employment, financial stability, physical health and the individual’s sense of morality may all be diminished as a consequence.
  2. Continuation in face of consequences: The user continues with the substance use even when threatened with significant losses as a direct consequence of continued use
  3. No control of consumption: A subjective sense of inability to control or restrict further consumption once the drug is taken
  4. Narrowed repertoire: The user moves from using a range of psychoactive substances to a single drug taken in preference to all others. Over time, the user tends to take the drug in the same setting with the same individuals and uses the same route of administration
  5. Rapid reinstatement of dependence follow abstinence: When the user relapses to drug use after a period of abstinence they are at risk of rapidly returning to the pattern of dependent use in a much shorter period of time.
  6. Tolerance and withdrawl: tolerance and physiological withdrawal symptoms are considered features of the dependence syndrome.
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4
Q

What is acute intoxication?

A

Transient physical and psychological abnormalities that occur following administration and are caused by the direct effects of the psychoactive substance.

Acute intoxication may cause disturbances in consciousness, cognition, perception, affect, behaviour or other psychophysiological functions.

The effects are specific and characteristic for each substance (e.g. disinhibition with alcohol, visual and sensory distortions with LSD).

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5
Q

What is the definition of withdrawal?

A

When there is physical dependence on a drug, abrupt stopping/ partial withdrawal of the substance generally leads to withdrawal symptoms.

The symptoms experienced and their severity and persistence usually relates to the type of substance and the quantity being used before stopping.

Some drugs are not associated with any withdrawal symptoms; some with mild symptoms only; others have significant withdrawal syndromes.

Clinically significant withdrawal symptoms are recognised in dependence on alcohol, opiates, benzodiazepines, cocaine and amphetamines.

Withdrawal syndromes can be simple or complicated by the development of seizures, delirium or psychotic symptoms.

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6
Q

What is the definition of tolerance?

A

Over time, the user finds that more of the drug must be taken to achieve the same intensity of pleasurable effects. They may attempt to combat increasing tolerance by choosing a more rapidly acting route of administration (e.g. intravenous rather than smoking).

Tolerant individuals are able to consume large quantities of the specific substance showing no or few signs of intoxication.

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7
Q

what is substance induced psychotic disorder?

A

Individual presents with psychotic symptoms (e.g. hallucinations and/or delusions) which occur as a direct result of substance-induced neurotoxicity.

Psychotic features may develop either during intoxication/ withdrawal states/ on a background of chronic harmful or dependent use.

It can be difficult to differentiate diagnostically between these individuals and those presenting with a primary psychotic illness (e.g. a psychotic episode in the context of schizophrenia).

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8
Q

What are the causes of alcohol dependence?

A
  1. Genetics: increased risk 7x if first degree relatives are alcohol dependent.
  2. Psychological factors- mental illness: depression, anxiety disorders, PD and schizophrenia increase risk of alcohol and substance misuse.
    •Stress, high social anxiety levels and low self-esteem are particularly associated with alcohol misuse
  3. Social/occupational: M more than F. More in low SES. Social isolation and loss of spouse. lower cost of alcohol also contributes. Certain jobs e.g. farming/ bartending.
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9
Q

What are the physical consequences of alcohol misuse?

A

Neuro:
CNS- cortical and subcortical atrophy with prominent white matter loss.
•Cognitive and memory impairment
•Reduction in brain weight and volume
•Wernicke-Korsakoff Syndrome- due to thiamine (B1) deficiency: amnesia, confusion, ataxia, opthalmoplegia.
•Central pontine myelinolysis (pseudobulbar palsy and quadriplegia)
•Cerebellar degeneration
Peripheral Nervous System
•Alcoholic peripheral neuropathy and myopathy
•Optic atrophy and visual changes

Resp: Increased susceptibility to infections and aspiration pneumonia
CVD: Increase chance arrhythmia (partic AF), stroke (haemorrhagic), cardiomyopathy, HT
Liver: fatty liver in >90% heavy drinkers, alcoholic hepatitis, cirrhosis- which may lead to splenomegaly (female more likely than male), HCC
Gastro/oesophageal: Mallory-Weiss tears, carcinoma, varicies, gastritis, PUD
GU: Hepatorenal syndrome if cirrhosis, HT cause CKD
GIT: malabsorption, diarrhoea, risk of lower GI ca
Reproductive: fertility issues, FAS if pregnant, hypogonadism (males), Erectile Dysfunction

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10
Q

What are the psychological consequences of alcohol misuse?

A

• alcoholic hallucinosis: rare in prolonged heavy use. Psychotic symptoms- auditory/tactile (usually) hallucinations in clear consciousness when sober that resolves on stopping drinking.
• cognitive impairment: 60% heavy drinkers will demonstrate CI when sober. Particularly affected are: short-term memory, long-term recall, new skill acquisition, executive functioning, but with relative preservation of IQ and language skills.
• pathological jealousy: delusional disorder in which patient believes partner is being/ has been unfaithful. Violence is associated with this delusion.
• depression + anxiety: significant association. alcohol may either be used to self-medicate for these issues/ may contrib to feeling depressed/ exacerbate anxiety in withdrawal.
suicide- rates higher in alcohol dependent individuals
schizophrenia is associated with alcohol misuse (i.e. higher rates than gen population)

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11
Q

What are the social consequences of alcohol misuse?

A
  • marital disharmony and divorce
  • DV
  • missed days of work and poor performance
  • financial and legal issues
  • risky sexual activity
  • psych harm to family members
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12
Q

What are the acute withdrawal symptoms and their RF?

A
they can range from mild to severe and life threatening, occur when those who are dependent on alcohol suddenly stop drinking. 
immediate onset (6-48h after last drink): seizures tonic clonic. RF- heavy long term drinker, previous withdrawal, epilepsy, hx head injury
mild symptoms (4-12h after last drink): anxiety, perspiration, nausea, insomnia, increase HR / BP, strong cravings
severe symptoms (2+ days after last drink): acute confusion, amnesia, psychomotor agitation, psychosis, Delirium Tremens.  
RF for more severe symptoms- end stage liver disease, comorbid infection e.g. pneumonia/ UTI, previous withdrawal episodes, long term and heavy drinking. 
Recommend low threshold for treating- for anyone at risk/ showing symptoms, and at risk of developing syndrome when admitted for other reasons.
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13
Q

What is Delirium Tremens?

A

•Medical emergency (up to 40% mortality if untx) which happens 1-7d after patient’s last drink in 5% patients.

•Symptoms include (in addition to symptoms of uncomplicated withdrawal):
◦Clouding of consciousness and disorientation to time, place and person
◦Amnesia for recent events
◦Hallucinations (visual, tactile- insects and auditory) and paranoid delusions
◦Severe sweating
◦Severe agitation
◦Severe psychomotor agitation and TREMOR
◦ High Fever, tachycardia, fluctuating BP
◦autonomic disturbances and electrolyte imbalances

•Differential: Alternative cause of delirium: head injury, hepatic/Wernicke encephalopathy, electrolyte disturbances, HF.

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14
Q

How is alcohol withdrawal managed?

A

Benzodiazepines for symptomatic relief and to reduce likelihood of seizures. Chlordiazepoxide for 7d (low abuse potential) on reducing regimen.
Close monitoring of physical and psych complications
Nutrition and vitamin supplementation- thiamine and vitamins

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15
Q

How is alcohol dependence managed?

A
  • Out Patient preferred due to lower cost and equal
    outcomes to an inpatient stay.
  • Use of Chlordiazepoxide
  • Oral Thiamine and multivitamins
    However, In Patient should be chosen if psychosis, physical frailty/ comorbid condition, past hx of severe withdrawal e.g. seizures, delirium, current psychiatric symptoms: delirium, confusion, psychosis, suicidality, severe biochem disturbances
  • 1 Chlordiazepoxide
  • 2 IV Pabrinex (Thiamine B1) to reduce risk of development of Wernicke’s Encepalopathy
  • Follow up and maintenance care. Pharma and psychosocial interventions.
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16
Q

What is the aetiology of Wernicke-Korsakoff Syndrome?

A

Due to neuronal degeneration because of thiamine (b1) deficiency most commonly seen in heavy drinkers.
Alcohol dependent individuals are particularly susceptible to thiamine deficiency:
•Heavy drinkers tend to have poor dietary habits and their vitamin intake is poor
•Chronic alcohol intake reduces thiamine absorption from the GI tract
•Many heavy drinkers have liver disease and the capacity for hepatic storage of thiamine is reduced

Wernicke’s encephalopathy and Korsakoff psychosis respectively represent the acute and chronic phases of a single disease process that can be halted before progression to Korsakoff’s

17
Q

What is Wernicke’s Encephalopathy? (include tx, prognosis, PC)

A

Due to neuronal degeneration because of thiamine (b1) deficiency most commonly seen in heavy drinkers.
Which results in gliosis and haemorrhage in grey matter of mammillary bodies, hypothalamus, midbrain.
Acute triad (not v common to see all 3 at once):
1.Acute confusional state – most common symptom of 3
2.Ocular-motor signs (ophthalmoplegia, nystagmus)
3.Ataxic gait
- Associated symptoms include peripheral neuropathy, resting tachycardia and stigmata of nutritional deficiency.
TX: IV Pabrinex (high potency B1 replacement therapy). Do not rehydrate with G containing solutions bc this will exacerbate B1 deficiency.
Treat concurrent alcohol withdrawal.
Prognosis
•If Wernicke’s encephalopathy is left untreated, approximately 80% of cases progress to Korsakoff syndrome
•Mortality is ~15% if left untreated

18
Q

What is Korsakoff Syndrome?

A

Chronic progression from Wernicke’s Encephalopathy - but not always, can present first in chronic stage.
Usually due to thiamine deficiency seen in heavy drinkers but can be secondary to head injury, carbon monoxide poisoning, or encephalitis.
Symptoms:
•Absence or significant impairment in ability to form new memories (anterograde amnesia)
•There may be some retrograde amnesia (but usually less marked)
•Confabulation - the person may describe false memories for a period for which they have amnesia
•Apathy: the patients lose interest in things quickly, and generally appear indifferent to change.
Tx
•Aggressively treat initial Wernicke’s encephalopathy if present
•Continue oral thiamine and multivitamins for up to two years
•Appropriate psychosocial interventions for cognitive impairment (e.g. occupational therapy input, carer support etc.)
Prognosis:
•20% of cases show complete recovery and 25% show significant recovery over time with the remainder largely showing no improvement

19
Q

What is the MOA and effect of Cocaine?

A

Serotonin reuptake inhibitor (antagonizes the transporter)
stimulant associated with feelings of extreme well-being, heightened mental and physical activity.
Stimulants- crack, amphetamines, MDMA.

20
Q

What is the MOA and effect of Heroin?

A

Agonizes mu opioid R, inhibiting GABA transmission, reducing the inhibitory effect of GABA on dopaminergic neurones

They have analgesic properties making the user feel
warmth, sedation and well-being

21
Q

what are the common comorbidities of substance misuse?

A
schizophrenia
PD
PTSD
Anxiety
Depression
GI disorders (partic liver)
CVD disease
Neurol disease
22
Q

What is dual diagnosis?

A

Dual diagnosis refers to people with a severe mental illness (including schizophrenia,
schizotypal and delusional disorders, bipolar affective disorder and severe
depressive episodes with or without psychotic episodes) combined with misuse of
substances (the use of legal or illicit drugs, including alcohol and medicine, in a way
that causes mental or physical damage). Prevalence rates of 20-37% in secondary mental health services and 6-15% in substance
misuse settings.

23
Q

What investigations should be done in substance misuse?

A

urine dip- find out what substances
FBC

Alcohol:

  • MCV - high specificity. Remains raised for 3-6 months after abstinence achieved due to lifespan of red blood cell
  • GGT - (sensitivity 20-90%) More specific than other LFTs for alcohol-related liver inflammation
  • Liver ultrasound scan if indicated
24
Q

What is the tx for Delirium Tremens?

A

First do investigations to rule out other causes of delirium e.g. Liver Failure, Head injury, Meningitis etc.

  1. Chlordiazepoxide IV
  2. IV Panrinex (Thiamine)
  3. Low stimulus environment, Frequent reassessment and monitoring
25
Q

What is Motivational Interviewing? (Principles and uses)

A

Core Principles:

  1. “Develop Discrepancy” Allowing patients to recognize dissonance between behaviour and their personal goals
  2. Rolling with Resistance- avoid direct confrontation
  3. Express Empathy- to establish good rapport with patient
  4. Support self efficacy- enhance their confidence to overcome barriers and their belief in their ability to succeed.
26
Q

What are some social interventions for substance misuse?

A

Housing Support

Financial support

27
Q

What is the epidemiology of alcohol misuse?

A

More than 9 million people in England regularly drink more than the recommended daily limits
Older tend to drink more regularly than younger but younger tend to binge. It is estimated that approximately 9% of UK adult men and 4% of UK adult women are dependent on alcohol

Alcohol was a particularly relevant factor in violent incidents between strangers, 64% of which were perceived to be alcohol related
Drink driving accounts for approximately 1 in 6 road accident deaths

28
Q

How would you assess alcohol use?

A

FAST or CAGE Screening tools
History: including current consumption- what, where, when, how much, how often. lifetime drinking- when started, when regular drinker, when thought had problem, any period of abstinence, withdrawal symptoms, tolerance signs, any memory loss, social/ occupational issues including forensic, any previous tx sought and relapse, mental health issues or physical issues that are resulting from or affected by drinking.

29
Q

What is the MOA of alcohol?

A

depressant- dampens CNS and reduces anxiety

similar to barbituates, cannabis, benzodiazepines